[Treatment of septic complications od secondary peritonitis].

The authors review the current management goals of surgical and antibiotic therapy in secondary peritonitis. Basic therapeutic regimen is the surgical elimination of the infectious source by means of a rational and risk-adapted operative procedure. Other technical procedures (such as intra- and postoperative lavage, drainage of the abdominal cavity, decompression, etc.

[Adjuvant regional arterial port chemotherapy after resection of colorectal liver metastases].

Between 1986 and 1995 we performed radical hepatic resections (R0 resections) in 109 patients with hepatic metastases following colorectal carcinoma. In 50 patients a hepatic arterial port device was implanted for adjuvant regional chemotherapy (HAI). Mitomycin C, 5-fluorouracil, and since 1993 folinic acid have been administered during 6 monthly repeated courses.

Modulation of pro- and antifibrinolytic properties of human peritoneal mesothelial cells by transforming growth factor beta1 (TGF-beta1), tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta).

A decreased fibrinolytic activity of serosal surfaces appears to be a major factor in the development of peritoneal fibrous adhesions. Serosal fibrinolysis is regulated by mesothelial release of tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor types 1 and 2 (PAI-1 and PAI-2). We investigated the influence of tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGF-beta1) and interleukin 1beta (IL-1beta) on pro- and antifibrinolytic properties of mesothelial cells (HOMC) using a cell/fibrin clot assay.

The influence of heat shock protein 70 induction on hemodynamic variables in a porcine model of recurrent endotoxemia.

The manipulation of stress gene expression by heavy metals provides protection against the lethal effects of endotoxemia in murine models of septic shock. These findings suggest that the increased resistance to endotoxin in vivo after stress protein induction could be explained by an attenuation of hemodynamic alterations and an altered pattern of inflammatory mediator release. Therefore, we measured main hemodynamic variables such as systemic and pulmonary artery pressure, cardiac output, heart rate, central venous pressure, and pulmonary artery wedge pressure, as well as the time-course of thromboxane-B2, 6-keto-PGF1 alpha, and interleukin 6 formation with and without induction of the stress response in an established porcine model of recurrent endotoxemia (Circ Shock 35:237-244, 1991).